The present invention pertains to a method and apparatus for treating congestive heart disease and related valvular dysfunction. More particularly, the present invention is directed to an adaptive cardiac constraint having an outer non-extentible device and a pair of inner inflatable members for preventing over-extension of the heart during diastole.
Congestive heart disease is a progressive and debilitating illness. The disease is characterized by a progressive enlargement of the heart. As the heart enlarges, the heart is performing an increasing amount of work in order to pump blood each heart beat. In time, the heart becomes so enlarged the heart cannot adequately supply blood. An afflicted patient is fatigued, unable to perform even simple exerting tasks and experiences pain and discomfort. Further, as the heart enlarges, the internal heart valves may not adequately close. This impairs the function of the valves and further reduces the heart""s ability to supply blood.
Causes of congestive heart failure (CHF) are not fully known. In certain instances, CHF may result from viral infections. In such cases, the heart may enlarge to such an extent that the adverse consequences of heart enlargement continue after the viral infection has passed and the disease continues its progressively debilitating course.
With initial reference to FIGS. 1 and 1A, a normal, healthy human heart Hxe2x80x2 is schematically shown in cross-section and will now be described in order to facilitate an understanding of the present invention. In FIG. 1, the heart Hxe2x80x2 is shown during systole (i.e., high left ventricular pressure). In FIG. 1A, the heart Hxe2x80x2 is shown during diastole (i.e., low left ventricular pressure).
The heart Hxe2x80x2 is a muscle having an outer wall or myocardium MYOxe2x80x2 and an internal wall or septum Sxe2x80x2. The heart Hxe2x80x2 has four internal heart chambers including a right atrium RAxe2x80x2, a left atrium LAxe2x80x2, a right ventricle RVxe2x80x2 and a left ventricle LVxe2x80x2. The heart Hxe2x80x2 has a length measured along a longitudinal axis BBxe2x80x2-AAxe2x80x2 from an upper end or base Bxe2x80x2 to a lower end or apex Axe2x80x2.
The right and left atria RAxe2x80x2, LAxe2x80x2 reside in an upper portion UPxe2x80x2 of the heart Hxe2x80x2 adjacent the base Bxe2x80x2. The right and left ventricles RVxe2x80x2, LVxe2x80x2 reside in a lower portion LPxe2x80x2 of the heart Hxe2x80x2 adjacent the apex Axe2x80x2. The ventricles RVxe2x80x2, LVxe2x80x2 terminate at ventricular lower extremities LExe2x80x2 adjacent the apex Axe2x80x2 and spaced therefrom by the thickness of the myocardium MYOxe2x80x2.
Due to the compound curves of the upper and lower portions UPxe2x80x2, LPxe2x80x2, the upper and lower portions UPxe2x80x2, LPxe2x80x2 meet at a circumferential groove commonly referred to as the A-V (atrio-ventricular) groove AVGxe2x80x2. Extending away from the upper portion UPxe2x80x2 are plurality of major blood vessels communicating with the chambers RAxe2x80x2, RVxe2x80x2, LAxe2x80x2, LVxe2x80x2. For ease of illustration, only the superior vena cava SVCxe2x80x2, inferior vena cava IVCxe2x80x2 and one of the left pulmonary vein LPVxe2x80x2 are shown as being representative.
The heart Hxe2x80x2 contains valves to regulate blood flow between the chambers RAxe2x80x2, RVxe2x80x2, LAxe2x80x2, LVxe2x80x2 and between the chambers and the major vessels, aorta and preliminary artery. For ease of illustration, not all of such valves are shown. Instead, only the tricuspid valve TVxe2x80x2 between the right atrium RAxe2x80x2 and right ventricle RVxe2x80x2 and the mitral valve MVxe2x80x2 between the left atrium LAxe2x80x2 and left ventricle LVxe2x80x2 are shown as being representative.
The valves are secured, in part, to the myocardium MYOxe2x80x2 in a region of the lower portion LPxe2x80x2 adjacent the A-V groove AVGxe2x80x2 and referred to as the valvular annulus VAxe2x80x2. The valves TVxe2x80x2 and MVxe2x80x2 open and close through the beating cycle of the heart H.
FIGS. 1 and 1A show a normal, healthy heart Hxe2x80x2 during systole and diastole, respectively. During systole (FIG. 1), the myocardium MYOxe2x80x2 is contracting and the heart assumes a shape including a generally conical lower portion LPxe2x80x2. During diastole (FIG. 1A), the heart Hxe2x80x2 is expanding and the conical shape of the lower portion LPxe2x80x2 bulges radically outwardly (relative to axis AAxe2x80x2-BBxe2x80x2).
The motion of the heart Hxe2x80x2 and the variation in the shape of the heart Hxe2x80x2 during contraction and expansion is complex. The amount of motion varies considerably throughout the heart Hxe2x80x2. The motion includes a component which is parallel to the axis AAxe2x80x2-BBxe2x80x2 (conveniently referred to as longitudinal expansion or contraction). The motion also includes a component perpendicular to the axis AAxe2x80x2-BBxe2x80x2 (conveniently referred to as circumferential expansion or contraction).
Having described a healthy heart Hxe2x80x2 during systole (FIG. 1) and diastole (FIG. 1A), comparison can now be made with a heart deformed by congestive heart disease. Such a heart H is shown in systole in FIG. 2 and in diastole in FIG. 2A. All elements of diseased heart H are labeled identically with similar elements of healthy heart Hxe2x80x2 except only for the omission of the apostrophe in order to distinguish diseased heart H from healthy heart Hxe2x80x2.
Comparing, FIGS. 1 and 2 (showing hearts Hxe2x80x2 and H during systole), the lower portion LP of the diseased heart H has lost the tapered conical shape of the lower portion LPxe2x80x2 of the healthy heart Hxe2x80x2. Instead, the lower portion LP of the diseased heart H dilates outwardly between the apex A and the A-V groove AVG. So deformed, the diseased heart H during systole (FIG. 2) resembles the healthy heart Hxe2x80x2 during diastole (FIG. 1A). During diastole (FIG. 2A), the deformation is even more extreme.
As a diseased heart H enlarges from the representation of FIGS. 1 and 1A to that of FIGS. 2 and 2A, the heart H becomes a progressively less efficient pump. Therefore, the heart H requires more energy to pump the same amount of blood. Continued progression of the disease results in the heart H being unable to supply adequate blood to the patient""s body and the patient becomes symptomatic of cardiac insufficiency.
For ease of illustration, the progression of congestive heart disease has been illustrated and described with reference to a progressive dilation of the lower portion LP of the heart H. While such enlargement of the lower portion LP is most common and troublesome, enlargement of the upper portion UP may also occur.
In addition to cardiac insufficiency, the enlargement of the heart H can lead to valvular disorders. As the circumference of the valvular annulus VA increases, the leaflets of the valves TV and MV may spread apart. After a certain amount of enlargement, the spreading may be so severe the leaflets cannot completely close. Incomplete closure results in valvular regurgitation contributing to an additional degradation in cardiac performance. While circumferential enlargement of the valvular annulus VA may contribute to valvular dysfunction as described, the separation of the valve leaflets is most commonly attributed to deformation of the geometry of the heart H.
Patients suffering from CHF are commonly grouped into four classes (i.e., Classes I, II, III and IV). In the early stages (e.g., Classes I and II), drug therapy is the most commonly prescribed treatment. Drug therapy treats the symptoms of the disease and may slow the progression of the disease. However, drugs may have adverse side effects. There is no cure for CHF; even with drug therapy, the disease will progress.
CHF is encountered with increasing frequency. Most of this increase can be attributed to the aging population. An estimated 4-5 million people in the United States have CHF with 400,000 new cases annually. This is an estimated 2,000 new cases annually per 1.5 million people. For those with advanced CHF, mortality is at an extremely high level with a 1-year mortality rate of 66%, and a 2-year mortality rate of 82%. The survival rate in patients with new onset heart failure after acute myocardial infarction is even lower, with only a small minority remaining alive after five years.
Thirty years ago, surgeons began actively developing techniques to treat pre-end stage CHF. Between 1967 and 1980, three unique clinical techniques were developed: heart transplantation, a mechanical assist system, and the artificial heart. The only permanent treatment for congestive heart disease is heart transplant.
Between 1985 and 1998, three other clinical options were developed: cardiomyoplasty, partial left ventriculectomy, and mechanical support devices such as plastic ventricular binding. Cardiomyoplasty is a treatment for earlier stage congestive heart disease (e.g., as early as Class III dilated cardiomyopathy). In this procedure, the latissimus dorsi muscle (taken from the patient""s back) is wrapped around the heart and chronically paced synchronously with ventricular systole. Pacing of the muscle results in muscle contraction to assist the contraction of the heart during systole.
Even though cardiomyoplasty has demonstrated symptomatic improvement, studies suggest the procedure only minimally improves cardiac performance. The procedure is highly invasive requiring harvesting a patient""s muscle and an open chest approach (i.e., sternotomy) to access the heart. Furthermore, the procedure is expensive, requires costly cardiomyostimulators, and is complicated. For example, it is difficult to adequately wrap the muscle around the heart with a satisfactory fit. Also, if adequate blood flow is not maintained to the wrapped muscle, the muscle may necrose. The muscle may stretch after wrapping, reducing its constraining benefits. Further, the muscle is generally not susceptible to post-operative adjustment. Finally, the muscle may fibrose and adhere to the heart causing undesirable constraint on the contraction of the heart during systole.
Partial left ventriculectomy is a surgical technique that includes dissecting and removing portions of the left ventricles in order to reduce heart volume. This radical new and experimental procedure subject to substantial controversy. Furthermore, the procedure is highly invasive, risky and expensive, and commonly includes other expensive procedures such as a concurrent heart valve replacement. This treatment is limited to Class IV patients, and accordingly, provides no hope to patients facing ineffective drug treatment prior to Class IV. If the procedure fails, emergency heart transplant is the only available option.
Despite the recent innovations, cardiac transplantation remains the technique of choice for the treatment of CHF. To qualify, a patient must be in the later stage of the disease (e.g., Classes III and IV, with Class IV patients given priority for transplant). Such patients are extremely sick individuals. Class III patients have marked physical activity limitation, and Class IV patients are symptomatic even at rest. Unfortunately, there is an inadequate supply of transplantable hearts for CHF patients. This increases the need for treatments that can bridge heart function between the time a heart is needed to the time a transplantable heart is available.
Mechanical support devices such as prosthetic heart binding are primarily used in intermediate procedures for treating congestive heart disease. Prosthetic cardiac binding is a procedure for applying a girdle to support a dilated heart. While still experimental, cardiac binding has promise for CHF patients.
For example, U.S. Pat. No. 5,702,343, dated Dec. 30, 1997, and U.S. Pat. No. 5,800,528, dated Sep. 1, 1998, teach a passive jacket to constrain cardiac expansion during diastole. These cardiac constraint devices can be placed on an enlarged heart and snugly fitted during diastole. However, such bindings are non-flexible and compress the diastolic heart at a constant pressure. If the diastolic heart is too tightly compressed during a single step procedure, it will likely arrest. Alternatively, if the diastolic heart is too weakly compressed during the single step procedure, initial positive results will revert to baseline heart failure after only several days. Performing multiple heart surgeries to gradually increase the pressure is not feasible.
A more flexible device is that seen in U.S. Pat. No. 6,193,648, dated Feb. 27, 2001. This device is a knit xe2x80x9cjacketxe2x80x9d that can be loosely slipped onto the heart. The heart may be pre-shrunk prior to placement of the device, or the device may be fitted on the heart without pre-shrinking the heart. The device is adjusted to a snug fit on the heart during diastole. Even though the device is more flexible, the disadvantage of this device is that it cannot be readjusted at a later date.
U.S. Pat. No. 6,206,820 dated Mar. 27, 2001, to Kazi, discloses a device for supporting cardiac function that is adaptable to the hemodynamic changes of the heart after surgery. However, this device is limited to only a selective part of the left ventricle of the heart, and only assists the heart during ventricle systole (contraction). The Kazi device does nothing for a failed heart during ventricular diastole because it cannot provide compression during diastole.
Accordingly, a need exists for a heart-binding device that can incrementally add compression to a failed heart during diastole to adjust to the hemodynamic changes of the heart over time.
A surgical method and device are disclosed for treating congestive heart disease. In general, an adaptive constraining device is placed on the heart. The device is a binding that covers the left and right ventricles, and which has an expandible chamber adjacent to each ventricle. The device allows the gradual increase of compression on the dilated heart while administering separate loads on the left and right ventricles. The gradual increase allows the heart to be hemodynamically remodeled so that the blood flow through the heart becomes more normal without the problems associated with the application of one-step compression.
By improving the hemodynamic function of the diseased heart by one-third to one-half, a reduction in the rate of one-year mortality for the patient is expected. In addition, days of hospitalization per year, and costs to government health systems for these patients, may be decreased by 75% or more due to reduced dependence on expensive drug therapy, improved mental function, and improved lifestyle.
While the present invention is particularly useful for case of heart failure, other applications are possible and references to use with diastolic heart failure of the ventricles should not be deemed to limit the application of the present invention. The present invention may be advantageously adapted for use where similar performance capabilities and characteristics are desired. These and other objects and advantages of the present invention will become apparent from the detailed description, claims, and accompanying drawings.